Immunoglobulin E levels and anticollagen antibodies in patients with postburn hypertrophic scars.

Immunoglobulin E (IgE) levels and eosinophil counts were measured in 18 former patients with burn injuries attending an outpatient clinic for hypertrophic scarring. In 15 of these 18 former patients with burns, IgG anticollagen antibodies were also measured. Earlier reports in the literature have suggested that a local immune reaction against collagen might play a role in enhancing inflammation, thereby increasing scar formation. In addition, we have previously reported an increase in allergic symptoms in patients with keloids and hypertrophic scars. Antibodies to the following collagen types were measured: human type I, human type III, bovine type I, and bovine type III. IgG anticollagen antibody levels were correlated with percentage third-degree burn, number of weeks after burn injury, and the patient's age. An increase in percentage third-degree burn and in number of weeks after burn injury was statistically significantly associated with an increase in serum anticollagen antibody level. Six of the 18 patients had higher than normal IgE levels (p value = 0.0002).

Correlation of hematologic markers of inflammation and lung function: a comparison of asymptomatic smokers and nonsmokers.

Increased inflammation of the peripheral airways has been implicated as a cause of pulmonary function impairment. However, little information is available on the correlation between subclinical decrements of pulmonary function and inflammation in asymptomatic individuals. A relationship between markers of inflammation and lung function may be useful in predicting the early onset of lung function impairment. The purpose of this study was to investigate the correlation of hematologic markers of inflammation and spirometry in asymptomatic smokers and nonsmokers. The specific objectives of this study were twofold. The first objective was to quantify and compare the spirometric measures of lung function in smokers and nonsmokers having similar demographic and lifestyle characteristics. The second objective was to define the correlation between these spirometric measurements and hematologic markers of inflammation (white blood cells, monocytes, basophils, PGE1, IgG, and IgE). Systemic blood samples and spirometric measurements were obtained from 61 age-matched (33 +/- 9 years) healthy, asymptomatic smokers and nonsmokers, with similar self reported lifestyles (i.e., food, alcohol, vitamin consumption and exercise). Both male and female smokers self reported a higher coffee consumption (P < 0.05) compared to nonsmokers. Male smokers self-reported a trend toward current blue-collar versus white-collar occupation when compared with the nonsmokers. Body weight (77.6 +/- 16.6 kg) did not differ between the smokers and nonsmokers. The male nonsmokers were taller than the male smokers (P < 0.05). All subjects were asymptomatic and had clinically normal spirometry. Compared to male nonsmokers, the male smokers had lower FEF25-75% and FEF75-45% values (P < 0.05). No additional spirometric measurements, including FEV1/FVC, FEV1 and FVC were significantly different. The female smokers did not differ from the female nonsmokers (P < 0.05) in any of the spirometric endpoints measured. Thirteen statistically significant (P < 0.05) correlations involving inflammatory (white blood cells, monocytes, basophils, and PGE1) or immunologic endpoints (IgE) and spirometric measurements were observed in female smokers, female nonsmokers and male nonsmokers. No statistically significant correlations involving immunologic or inflammatory endpoints were observed in the male smokers. A better mechanistic understanding of the observed relationship between elevated hematologic inflammatory endpoints and reduced lung function may provide valuable insight into the clinical significance of these correlations.

Blood parameters associated with atherogenic and thrombogenic risk in smokers and nonsmokers with similar life-styles.

Current evidence indicates that life-style factors can affect the risk of developing cardiovascular disease. The life-style of cigarette smokers, as a group, differs in many ways from that of nonsmokers. Most studies that compare clinical pathologic findings related to atherogenic and thrombogenic risk in smokers and nonsmokers do not adequately control for most of the life-style differences between these two groups. In this study, a number of atherogenic risk factors (cholesterol, low-density lipoprotein, high-density lipoprotein, very low-density lipoprotein, high-density lipoprotein/cholesterol, triglycerides, and glucose) and thrombogenic risk factors (total white blood cell count, total red blood cell count; percent of monocytes, lymphocytes, neutrophils, basophils, and eosinophils; interleukin-1, leukotriene B4, hematocrit, hemoglobin, bilirubin, mean corpuscular hemoglobin, mean corpuscular hemoglobin concentration, mean corpuscular volume, platelet count, prothrombin time, partial thromboplastin time, and fibrinogen) were compared in male and female cigarette smokers and non-smokers who were selected to have approximately similar self-reported life-styles (i.e., food, alcohol, and vitamin consumption and exercise level). However, the smokers (male and female) consumed more coffee (P < 0.05) than the nonsmokers. A trend toward blue-collar versus white collar occupational status was also observed in the male smokers relative to male nonsmokers. Cigarette consumption and urinary cotinine and carboxyhemoglobin levels did not differ between male and female smokers. Atherogenic and thrombogenic values were determined from venous blood samples. No statistically significant (P > 0.05) differences in clinical pathologic findings related to atherogenic risk were observed between the smokers and nonsmokers.(ABSTRACT TRUNCATED AT 250 WORDS)

A comparison of the mutagenicity of mainstream cigarette smoke condensates from a representative sample of the U.S. cigarette market with a Kentucky reference cigarette (K1R4F).

The Salmonella mutagenicity assay has been used to investigate the mutagenicity of cigarette smoke and cigarette smoke condensate. The Kentucky reference (K1R4F) cigarette is designed to be representative of full-flavor, low-tar cigarettes sold in the U.S. and to serve as a reference standard for comparative studies on the chemistry and biological activities of cigarette smoke and condensate. The objective of this study was to determine if the mutagenicity of mainstream smoke condensate from the K1R4F, as measured by the Salmonella mutagenicity assay, is representative of the mutagenic activity of U.S. cigarettes. Mainstream smoke condensates prepared in dimethyl sulfoxide from the K1R4F and 73 brand styles (representing greater than 70% of the total U.S. cigarette market) were assayed using Salmonella typhimurium TA98 and TA100 (+S9) at concentrations of 0, 25, 50, 75, 100, 125 and 250 micrograms/plate. Revertants/mg condensate were determined by calculating the slopes of the dose-response curves using linear and nonlinear regression models. Revertants/cigarette were determined by multiplying the revertants/mg condensate by the mg condensate/cigarette. No significant differences (p > 0.05) were observed between the mean mutagenicity of U.S. market and K1R4F mainstream smoke condensates in terms of revertants/mg condensate or revertants/cigarette. Increased variability in mutagenicity was observed among the U.S. brands versus that of the K1R4F. This is not surprising since variability among the U.S. brands would be expected to have both measurement error and brand style variability while the K1R4F variability contains only the measurement error portion. These results demonstrate that the K1R4F is a representative model for the U.S. cigarette market in comparative Salmonella mutagenicity studies using mainstream smoke condensates.